Endocrine

What is considered to be the most postent stimulator for endocrine hormones

as glucose drops, cortisol rises.

A prolactin secreting adenoma. *LACTOTROPE*

they are very common, and usually asymptomatic

multiple endocrine neoplasia syndrome. These pts are at increased risk for adenomas of the pituitary, parathyroid gland, and pancreas (THE THREE P's)

G protein mutations (GNAS).

Lactotrophs: prolocatinoma, Somatotroph: GH secreting adenoma, corticotrophs: cushing's disease, gonadotrophs: gonadotropin secreting adenoma, and thyrotrophs: TSH secreting adenoma

Pregnancy, primary hypothyroidism (incresaed TSH leading to prolactin increase), stress and corticosteroid tx, DA receptor antagonists, chronic renal failure, idiopathic, stalk disconnection, acromegally

bone demineralization due to loss of estrogen effect (decreased estrogen due to supression of GnRH

chromophobe

most of them are benign. Only considered malignant *IF THEY METASTASIZE*. Malignancy cannot be determined by cytology, only by metastasis

dopamine agonist: bromocriptine or cabergoline. surgical resection or radiotherapy may also be used if warranted

because GH inhibits insuline release.

GH secreting adenoma. It would also be noted that glucose levels would spike more, for a longer period of time, as compared to a normal pt. Relationship b/w GH and glucose should inverse, due to insulin response.

somatostatin analogue to shrink tumor in preparation for surgical removal

GH does not act directly on tissues. It is first converted to IGF-1 in the liver, which in turn acts on target tissues.

The active form of GH. GH itself does not act directly on tissue, it acts via IGF-1

synergize with cortisol and antagonize insuline (insuline resistance), increase lipolysis, increase glycogenolysis and gluconeogenesis, increase GFR leading to increase sodium and H2O retention (HTN!!!). increase BMR and thyroxin (T3)

Densely granulated (SLOW GROWING) - STRONGLY POSITIVE FOR GH. and sparsely granulated (FAST GROWING) MADE OF KERATIN 8. Cells show cellular and nuclear pleomorphism

postpartum hypopituitarism due to necrosis of the anteriod pituitary, The necrosis is caused by severe bleeding and hypoperfusion during delivery. Presents with fatigue, anorexia, poor lactation, and loss of hair all over body.

There is no direct arterial blood supply to the anterior pituitary, instead there is a low pressure portal vein system. THis prevents large amount of hormones from being leaked out constantly.

hormone supplimentation. TSH is replaced by *L-thyroxine*, cortisone is given po, and testosterone must be given to men. IGF-1 is given to replace GH.

FSH/LH

growth chart, IGF-1, and bone age (X-ray of left hand

ADH

rarely due to pituitary pathology. Most always due paraneoplastic syndrome, etc

dilutional hyponatremia due to excess water resorption. K+ is normal or slightly decreased because the hypokalemia is compensated by a shift of extracellular H+ for intracellualar K+. pH of urine is normal because of the h+ reabsorption

restricting water intake to normalized the ADH levels

Post pituitary (neurohypophesis): vasopressin (ADH) and oxytosin (made in the hypothalamus and shipped to the post pit. Ant Pituitary: FSH, LH, ACTH, TSH, Prolactin, GH (FLAT PIG) and MSH

ADH (AKA vasopressin) is secreted from the hypothalamus into the post. pituitary, where it is secreted.

Thickened, dark, hyperpigmented area of skin seen in area of friction such as the neck, belt lines, or medial aspect of thigh. Common in TYPE II DM (AKA insulin resistant)

high blood sugar results in higher osmostic pressure within the lens which draws in water, causing swelling of the lens

Glucagon

GLP-1 and GIP Incretins are gastrointestinal hormones that increase insulin released from beta cells of pancrease (islet of langerhans) even before glucose levels increase. They also inhibit glucagon release.

GLP-1

GLP-1

Because they don't produce enough incretins (GLP-1 and GIP) so gastric emptying is too fast (due to asbsence of GLP-1) and satiety is not signalled (Also due to absence go GLP-1). They also have dcreasd B-Betacell funct due to lack of incretin stim.

amyloid deposits in the pancrease. Apple green perfringence on viewing with polarized light... stains red with congo red stain.

alpha cells secrete glucagon. Stimilated by free fatty acids.

Alpha cells of pancreas.

FASTING GLUCOSE: 100-125 = Impaired fasting glucose, 126 and up= diabetic. Normal is under 100. 2 hour post glucose load = normal under 140, diabetic if over 200, impaired tolerance if 141-200.

FBS 126 and up, RBS 200 and up. ABNORMAL HbA1c cannot be used to diagnosis of DM

MI. Increased risk by 50%, which is same risk increase as someone who has already had an MI

lifestyle modifcation. *Build muscle, lose fat*, change diet.

hyperglycermia (>250)

cytotoxic T-cells (CD8+) and Th1 (CD4+) . Antigen is unknown.

type II is asso with infections, type I is asso with DKA

type II. Concordance = frequency of occurence in identical twins. Type I is likely to be due to environmental factors in addition to a minor role with genetics.

1) IV fluids to rehydrate, correct osmolarity and acidosis (by flushing out ketones). 2) insulin to decrease ketone formation (lipolysis) and correct acidosis. (continue till acidosis is resolved). 3) replace K. Give mannitol to tx cerebral edema

glucose in liquid form. If they are unconscious give glucagon or IV glucose.

diabetes due to severe exocrine pancrease dysfunction. (cystic fibrosis related diabetes (CFRD)

Maturity Onset Diabetes of Young. type of diabetes seen in non-obese kids due to monogenetic mutation in GLUCOKINASE OR HAPTIC NUCLEAR FACTOR 1 or 2. Presents as nonketotic form of DM w/o islet cell ABs. Often asso with a fam hx of DM over several gens

MODY

mutation in glucokinase or hepatic nuclear factor 1 or 2

4.0-6.0%

NON-ENZYMATIC GLYCOSYLATION is athe core of all pathology. Formation of advanced glycosylation products, activation of PKC and angiogenic pathways, IC disturbances in polyol pathway (neoropathy, cateracts, etc) CAUSES MACROANGIOPATHY AND MICROANGIOPATHY

ALong with high glucose, diabetics also have higher free fatty acids,,, this leads to atherosclerosis and increased risk of MI.

depostion of advanced glycosylation products due to non-enzymatic glycosylation!

AGEs cause changes to basement membrane / pericyte degeneration leading to ischemia. This triggers VEGF mediated angiogenesis of leaky vessels which hemorrhage.

5-10%

Hyperplasia of the beta cells due to transplacental effects of glucose at high levels in mother. Hyperplasia in beta cells leads to higher than normal insulin levels.

the "P" organs: pancrease, pituitary, and parathyroid overactivity. AD inheritence. (elevated gastin (from pancrease), calcium and parathyroid hormone elevation.

MEN1

Chief cells, water clear cells, and oxyphil cells

Calcitonin increased calcium uptake in the bones by lowering serum Ca2+. IT IS SECRETED BY THE THYROID GLAND. This hormone is opposed by PTH which increases osteoclast acitivity, thus increasing serum Ca++ by increasing bone resorption

Stims osteoclastic resorption/inhibits osteoblastic bone formation.2) increases ca++ reabsorption in the kidney while blocking phosphate reabsorption. 3) INCREASES 1-hydroxylation 25-hydroxy vitamin D in the PCT epith. -> 1,25-dihydroxyvitamine D

1,25-dihydroxyvitamin D (Calcetriol). PTH facilitates its formation by converting 25-hydroxy vitamin D

formation of a neoplasia in the presence of a secondary hyperparathyroidism induced hyperplasia

primary: hypersecretion of PTH by an adenoma or hyperplasia Secondary: Physiologic increase in PTH in response to hypocalcemia. Tertiary: development of autonomatous hypersecreting adenoma in longstanding 2ry hyperparathyroidism

a primary adenoma.

Primary is due to a primary adenoma, tertiary is due to an adenoma that arises in a patient with SECONDARY DISEASE.

hypocalcemia. THe kidney confuses these two ions. so: Hypomagnesemia is a cause of hyperparathyroidism

Phosphate.

HYPERCALCEMIA and HYPOPHOSPHATEMIA

painful bones, renal stones, abdominal groans (pancreatitis) and mental moans

If only one parathyroid gland is enlarged, its an adenoma. If all 4 are enlarged, it is hyperplasia

Hyperplastic parathyroid has more areas of fat.

metastatis.

brown tumor of bone caused by hyperparathyroidism

Hyperparathyroidism, paraneoplastic phenomenon, malignancy with bone mets, and thiazide diuretic use. (lithium use, hypervitiminosis D, etc are rarer causes)

Increased serum calcium levels and raised PTH levels with decreased plasma phosphate and mild metabolic acidosis. THis is confirmed with a SPECT scan of the parathyroid gland.

Decreased Ca++ amd increased PTH

Chronic renal failure leading to decreased levels of calcium and *calcitriol* leads to increased PHT --> increased bone resorption and decreased bone remodeling. Also decreased Vitamin D production --> osteolamalasia.

decreased vitamin D synthesis

MEN tumors and RET gene mutations

Twitching of facial muscles after tapping the facial nerve just in front of the ear. Indicative of hypoparathyroidism.

Low or absent PTH, hypocalcemia, hyperphosphatemia.

Hyperexcitability; hypocalcemia. Hypoexcitability;hypercalcemia (hyperparathyroid

pseudohypoparathyroidism (Parathyroid resistance). Urinary cAMP fails to rise in response to PTH administration

Obese patient with various skeletal abormalities, bachydactly, potters thumb, and dimples over knuckles when fist is clenched.

MEN syndrome (Multiple Endocrine Neoplasia)

Thyrid Binding Globulin

T4: increased, T3: Increased, T3RU: Increased

T4: decreased, T3: decreased, T3RU: decreased

T4: increased, TOTAL T3: Increased, T3RU: decreased

T4: decreased, T3: decreased, T3RU: increased

Hyperfunctioning nodules will take up isotope... the are hot nodules. Non-functioning nodules will not take up isotope... these are cold nodules. Cold nodules are more likely to cary malignancy, but overall majority of nodules are benign

Follicular adenoma. it is composed of follicular adenomas (thyroid follices) It presents as a COLD NODULE. Most common 40-60 yo. Has no potential to turn malignant.